Not so sweet and simple: impacts of SARS-CoV-2 on the β cell

被引:15
作者
Ibrahim, Sarah [1 ,2 ]
Monaco, Gabriela S. F. [2 ]
Sims, Emily K. [2 ,3 ,4 ]
机构
[1] Indiana Univ Sch Med, Biochem & Mol Biol, Indianapolis, IN 46202 USA
[2] Indiana Univ Sch Med, Ctr Diabet & Metab Dis, 635 Barnhill Dr MS 2031E, Indianapolis, IN 46202 USA
[3] Indiana Univ Sch Med, Wells Ctr Pediat Res, Indianapolis, IN 46202 USA
[4] Indiana Univ Sch Med, Pediat Endocrinol & Diabetol, Indianapolis, IN 46202 USA
关键词
COVID; SARS-CoV-2; diabetes; islet; beta cell; SEVERE ACUTE-PANCREATITIS; TYPE-2; DIABETES-MELLITUS; CYTOKINE STORM; GLYCEMIC CONTROL; ENTRY FACTORS; COVID-19; ACE2; INFLAMMATION; CORONAVIRUS; MECHANISMS;
D O I
10.1080/19382014.2021.1909970
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The link between COVID-19 infection and diabetes has been explored in several studies since the start of the pandemic, with associations between comorbid diabetes and poorer prognosis in patients infected with the virus and reports of diabetic ketoacidosis occurring with COVID-19 infection. As such, significant interest has been generated surrounding mechanisms by which the virus may exert effects on the pancreatic beta cells. In this review, we consider possible routes by which SARS-CoV-2 may impact beta cells. Specifically, we outline data that either support or argue against the idea of direct infection and injury of beta cells by SARS-CoV-2. We also discuss beta cell damage due to a "bystander" effect in which infection with the virus leads to damage to surrounding tissues that are essential for beta cell survival and function, such as the pancreatic microvasculature and exocrine tissue. Studies elucidating the provocation of a cytokine storm following COVID-19 infection and potential impacts of systemic inflammation and increases in insulin resistance on beta cells are also reviewed. Finally, we summarize the existing clinical data surrounding diabetes incidence since the start of the COVID-19 pandemic.
引用
收藏
页码:66 / 79
页数:14
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